Beneficial effects of fluid resuscitation via the rectum on hemodynamic disorders and multiple organ injuries in an experimental severe acute pancreatitis model

Pancreatology ◽  
2015 ◽  
Vol 15 (6) ◽  
pp. 626-634 ◽  
Author(s):  
Ying Chen ◽  
Li Ma ◽  
Xiaoqin Song ◽  
Jian Fei ◽  
Erzhen Chen ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Fluid Resuscitation ◽  
Multiple Organ ◽  
Beneficial Effects

scholarly journals Protective Effects of Emodin-Induced Neutrophil Apoptosis via the Ca2+-Caspase 12 Pathway against SIRS in Rats with Severe Acute Pancreatitis

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Gui-Jun Wang ◽  
Yue Wang ◽  
Yong-Sheng Teng ◽  
Fa-Lv Sun ◽  
Hong Xiang ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Multiple Organ ◽  
Neutrophil Apoptosis ◽  
Protective Effects ◽  
Expression Levels ◽  
Beneficial Effects ◽  
Caspase 12 ◽  
Underlying Mechanisms ◽  
Active Fragments

Severe acute pancreatitis (SAP) results in high mortality. This is partly because of early multiple organ dysfunction syndromes that are usually caused by systemic inflammatory response syndrome (SIRS). Many studies have reported the beneficial effects of emodin against SAP with SIRS. However, the exact mechanism underlying the effect of emodin remains unclear. This study was designed to explore the protective effects and underlying mechanisms of emodin against SIRS in rats with SAP. In the present study, cytosolic Ca2+ levels, calpain 1 activity, and the expression levels of the active fragments of caspases 12 and 3 decreased in neutrophils from rats with SAP and increased after treatment with emodin. Delayed neutrophil apoptosis occurred in rats with SAP and emodin was able to reverse this delayed apoptosis and inhibit SIRS. The effect of emodin on calpain 1 activity, the expression levels of the active fragments of caspases 12 and 3, neutrophil apoptosis, and SIRS scores were attenuated by PD150606 (an inhibitor of calpain). These results suggest that emodin inhibits SIRS in rats with SAP by inducing circulating neutrophil apoptosis via the Ca2+-calpain 1-caspase 12-caspase 3 signaling pathway.

Multiple organ dysfunction associated with severe acute pancreatitis (SAP)

2001 ◽  
Vol 120 (5) ◽  
pp. A644-A645
Author(s):  
Kimmo I. Halonen ◽  
Ville Pettila ◽  
Ari K. Leppaniemi ◽  
Esko A. Kemppainen ◽  
Pauli A. Puolakkainen ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Organ Dysfunction ◽  
Severe Acute Pancreatitis ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction

scholarly journals NLRP3 Deficiency Alleviates Severe Acute Pancreatitis and Pancreatitis-Associated Lung Injury in a Mouse Model

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Qiang Fu ◽  
Zhensheng Zhai ◽  
Yuzhu Wang ◽  
Lixia Xu ◽  
Pengchong Jia ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Lung Injury ◽  
Severe Acute Pancreatitis ◽  
Nlrp3 Inflammasome ◽  
Early Death ◽  
Neutrophil Infiltration ◽  
Multiple Organ ◽  
Dependent Manner ◽  
Dose Dependent ◽  
Nlrp3 Expression

The rapid production and release of a large number of inflammatory cytokines can cause excessive local and systemic inflammation in severe acute pancreatitis (SAP) and multiple organ dysfunction syndrome (MODS), especially pancreatitis-associated acute lung injury (P-ALI), which is the main cause of early death in patients with SAP. The NLRP3 inflammasome plays an important role in the maturation of IL-1β and the inflammatory cascade. Here, we established a model of SAP using wild-type (NLRP3+/+) and NLRP3 knockout (NLRP3-/-) mice by intraperitoneal injections of caerulein (Cae) and lipopolysaccharide (LPS). Pathological injury to the pancreas and lungs, the inflammatory response, and neutrophil infiltration were significantly mitigated in NLRP3-/- mice. Furthermore, INF-39, an NLRP3 inflammasome inhibitor, could reduce the severity of SAP and P-ALI in a dose-dependent manner. Our results suggested that SAP and P-ALI were alleviated by NLRP3 deficiency in mice, and thus, reducing NLRP3 expression may mitigate SAP-associated inflammation and P-ALI.

scholarly journals Minimally invasive drainage versus open surgical debridement in SAP/SMAP – a network meta-analysis

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Kai Zhang ◽  
Xiaole Zhu ◽  
Chaoqun Hou ◽  
Chenyuan Shi ◽  
Yi Miao ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Minimally Invasive ◽  
Severe Acute Pancreatitis ◽  
Meta Analysis ◽  
Multiple Organ ◽  
Surgical Debridement ◽  
Percutaneous Catheter Drainage ◽  
Endoscopic Drainage ◽  
Percutaneous Catheter ◽  
Study Participants

Abstract Background The efficacy of some therapeutic methods (open surgical debridement (OSD), conservative treatment (CST) and minimally invasive drainage (MID)) for severe acute pancreatitis (SAP) and moderately severe acute pancreatitis (MSAP) has been widely evaluated. However, the results remained controversial. We performed this study to illuminate whether any difference in incidence exists on patients with SAP/MSAP treated with OSD and MID. Methods Eligible articles were collected base of a comprehensive review of PUBMED, EMBASE, COCHRANE, CKNI and WANGFANG for published randomized controlled trials. Two steps of meta-analysis were performed, routine pair-wise meta-analysis and network meta-analysis. Results Thirteen studies were included in this study. Participants were classed as 5 groups, CST, early MID (EMID), late MID (LMID), early OSD (EOSD) and late OSD (LOSD). And MID contains endoscopic drainage (ESD), percutaneous catheter drainage (PCD) and minimally invasive surgery (MIS). Compared with CST, MID could decrease both mortality and multiple organ dysfunction syndrome (MODS) rate but OSD couldn’t. Both EMID and MID can significantly decrease the mortality and MODS rate compared to CST. PCD might be most likely to have a benefit compared to CST. Conclusion Existing evidence for the use of MID in SAP/MSAP is reliable and it can be used as early treatment. OSD, if necessary, should be avoided or delayed as long as possible.

scholarly journals Protective Effect of Tetrandrine on Sodium Taurocholate-Induced Severe Acute Pancreatitis

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Xian-lin Wu ◽  
Jie-xing Li ◽  
Zhen-dong Li ◽  
Da-sheng Liu ◽  
Su-hong Lu ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Free Radical ◽  
Bile Duct ◽  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Protective Effect ◽  
Severe Acute Pancreatitis ◽  
Sodium Taurocholate ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction

Tet is a type of alkaloid extracted fromStephania tetrandra, and it has recently been demonstrated that Tet can protect against inflammation and free radical injury and inhibit the release of inflammatory mediators. The present study was designed to observe the protective effect of Tet on sodium taurocholate-induced severe acute pancreatitis (SAP). The rat model of SAP was induced by retrograde bile duct injection of sodium taurocholate and then treated with Verapamil and Tet. The results showed that Tet can reduce NF-κB activation in pancreas issue, inhibit the SAP cascade, and improve SAP through inducing pancreas acinar cell apoptosis and stabilizing intracellular calcium in the pancreas, thus mitigating the damage to the pancreas. Our study revealed that Tet may reduce systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndromes (MODS) to protect against damage, and these roles may be mediated through the NF-κB pathway to improve the proinflammatory/anti-inflammatory imbalance.

scholarly journals Targeting neutrophil extracellular traps in severe acute pancreatitis treatment

2020 ◽  
Vol 13 ◽  
pp. 175628482097491
Author(s):  
Jing Hu ◽  
Hongxin Kang ◽  
Huan Chen ◽  
Jiaqi Yao ◽  
Xiaolin Yi ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Inflammatory Cells ◽  
Neutrophil Extracellular Traps ◽  
Multiple Organ ◽  
Organ Injury ◽  
Normal Tissues ◽  
Pathogen Invasion ◽  
Extracellular Traps ◽  
Abdominal Disease

Severe acute pancreatitis (SAP) is a critical abdominal disease associated with high death rates. A systemic inflammatory response promotes disease progression, resulting in multiple organ dysfunction. The functions of neutrophils in the pathology of SAP have been presumed traditionally to be activation of chemokine and cytokine cascades accompanying the inflammatory process. Recently, since their discovery, a new type of antimicrobial mechanism, neutrophil extracellular traps (NETs), and their role in SAP, has attracted widespread attention from the scientific community. Significantly different from phagocytosis and degranulation, NETs kill extracellular microorganisms by releasing DNA fibers decorated with granular proteins. In addition to their strong antimicrobial functions, NETs participate in the pathophysiological process of many noninfectious diseases. In SAP, NETs injure normal tissues under inflammatory stress, which is associated with the activation of inflammatory cells, to cause an inflammatory cascade, and SAP products also trigger NET formation. Thus, due to the interaction between NET generation and SAP, a treatment targeting NETs might become a key point in SAP therapy. In this review, we summarize the mechanism of NETs in protecting the host from pathogen invasion, the stimulus that triggers NET formation, organ injury associated with SAP involving NETs, methods to interrupt the harmful effects of NETs, and different therapeutic strategies to preserve the organ function of patients with SAP by targeting NETs.

scholarly journals Interventional Treatment of Abdominal Compartment Syndrome during Severe Acute Pancreatitis: Current Status and Historical Perspective

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Dejan V. Radenkovic ◽  
Colin D. Johnson ◽  
Natasa Milic ◽  
Pavle Gregoric ◽  
Nenad Ivancevic ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Conservative Treatment ◽  
Compartment Syndrome ◽  
Abdominal Compartment Syndrome ◽  
Severe Acute Pancreatitis ◽  
Fluid Resuscitation ◽  
Interventional Treatment ◽  
Invasive Approach ◽  
Aggressive Fluid Resuscitation ◽  
Abdominal Compartment

Abdominal compartment syndrome (ACS) in patients with severe acute pancreatitis (SAP) is a marker of severe disease. It occurs as combination of inflammation of retroperitoneum, visceral edema, ascites, acute peripancreatic fluid collections, paralytic ileus, and aggressive fluid resuscitation. The frequency of ACS in SAP may be rising due to more aggressive fluid resuscitation, a trend towards conservative treatment, and attempts to use a minimally invasive approach. There remains uncertainty about the most appropriate surgical technique for the treatment of ACS in SAP. Some unresolved questions remain including medical treatment, indications, timing, and interventional techniques. This review will focus on interventional treatment of this serious condition. First line therapy is conservative treatment aiming to decrease IAP and to restore organ dysfunction. If nonoperative measures are not effective, early abdominal decompression is mandatory. Midline laparostomy seems to be method of choice. Since it carries significant morbidity we need randomized studies to establish firm advantages over other described techniques. After ACS resolves efforts should be made to achieve early primary fascia closure. Additional data are necessary to resolve uncertainties regarding ideal timing and indication for operative treatment.

Sign in / Sign up

Export Citation Format

Share Document